The Immune System and Multiple Sclerosis

In a healthy body, nerve fibers (also referred to as “axons“) have a protective, fatty-rich protein covering known as myelin. This covering insulates the nerve fibers, similar to the insulating rubber covering of an electric wire. Myelin allows for the smooth and uninterrupted flow of nerve impulses, which in turn, enables the body to send vital instructions from the brain to the different parts of the body.

With multiple sclerosis (MS), the body’s own system of defense, known as the immune system, malfunctions. It sends disease-fighting cells into the central nervous system (CNS) that may destroy the body’s own myelin. This occurs because the immune system is incorrectly identifying the myelin in the CNS as a foreign body. When the body’s own immune system attacks its own tissue, this is referred to as an “autoimmune disease,” and MS is believed to fall into this category. Examples of other autoimmune diseases include lupus and rheumatoid arthritis.

These renderings of the inside of a blood vessel show normal red blood cells, along with immune-system cells that are designed to fight infection and disease. With ms, these cells of the immune system are thought to become misdirected and attack the body’s own tissues – in this case, the nerves of the cns. In order to reach the cns, these immune-system cells must cross the blood-brain barrier – traveling through the blood vessel wall and into the brain and spinal cord.

Lymphocytes are a type of white blood cell and play a strong role in the body’s defense system. Another type of white blood cell is the macrophage, and this works to ingest and destroy foreign substances.

White blood cells circulate in the blood and are produced when the immune system perceives a foreign body and instructs the cells to eliminate it, thereby “protecting” the body. In order to reach the nerves within the CNS, the immune system cells and molecules must cross a protective barrier that surrounds the blood vessels. Known as the blood-brain barrier (BBB), this layer of cells is designed to prevent damaging cells and other substances in the blood (including those that could cause disease) from entering the brain, optic nerves, and spinal cord of the CNS.

With MS, damaging immune-system cells are able to break through the BBB and enter the CNS, where they begin their attack on the myelin. Once the damaging cells enter the CNS, macrophages and other lymphocytes begin their attack on the myelin. This creates inflammation along the nerves where the myelin is being damaged. Areas of activity are known as lesions (or plaques). Lesions vary in activity levels, ranging from very active (acute), to chronic, to inactive.

Remyelination is believed to occur in relapsing-remitting MS (RRMS) when a symptom flare-up subsides and goes into remission. The return of function is thought to result from not only myelin repair, but reduced inflammation as well. Eventually, the axon becomes exposed and damaged, and the myelin may no longer be repaired. With primary-progressive MS (PPMS) and other forms of progressive MS, the oligodendrocytes are unable to repair the myelin, and therefore symptoms do not remit.

Shown above is a 3-D rendering of nerve cells; the axon and protective myelin can easily be seen extending out to the side of the cell body.

Often, myelin that is damaged may be restored through a process called “remyelination,” particularly early in the disease. Oligodendrocytes are cells that produce and maintain myelin. Over time, however, oligodendrocytes may be lost and unable to repair the damaged myelin.

Areas of damaged myelin become scarred and can no longer fully insulate the nerve – leaving unprotected areas, where the flow of nerve impulses is interrupted. This interruption in the communication between the brain and other parts of the body results in the symptoms experienced by individuals with MS.